FWD>RE>New aging insights i

Mail*Link( SMTP FWD>RE>New aging insights in Science?
The Werner's gene appears to be a DNA helicase, not SOD. In general terms,
the observation suggests that when the helicase is knocked out in Werner's
syndrome, cells accumulate DNA damage resulting in premature cell senescence
with the clinical result being premature onset of age-related disease. Since
the gene is obviously normal in everyone else, the interesting question is
what sort of DNA damage looks similar to that generated by the elimination of
this helicase. One possibility proposed in the Science paper was the
attrition of telomeric DNA with replicative senescence. Alternatively, it
could be other kinds of DNA damage... The take home lesson may be that the
integrity of the DNA is critical in the aging process.
-MWest
--------------------------------------
Date: 4/24/96 1:04 PM
From: Jason Taylor
Todd A Carter (tac2 at ahnnyong.cc.columbia.edu) wrote:
: In article <NEWTNews.829377280.29969.yeger at m1.sprynet.com.sprynet.com>,
: <yeger at m1.sprynet.com> wrote:
: >
: >The front of the Wall Street Journal had a blurb to the effect that
: >researchers discovered the gene that causes Werner's syndrome, a disease
: >marked by premature ageing, that it boosts insights into normal aging, and
: >that the results are published in Science. I got the April 5 issue today
and
: >didn't find anything. Anyone know anything about this?
For what its worth, I remember skimming the articles. There were two
of them. All I remember for sure is that the articles were too
general and short to really say anything. One of them showed a
picture of a ~40 year old Chinese woman who looked ~70. (Is Science
going the MTV lets-show-pictures-of-people-instead-of-data route as
well? What's happening?) Wait ... I think do recall one of them
saying that this was the first genetic disease that was indirectly
uncovered by the human genome project. I suppose a sceptic of the
free radical theory of aging would not like the new result, since if I
recall correctly the gene codes something like SOD. (Almost all
traditional symptoms of aging except heart disease and Alzheimer's
show up in these patients, so obviously if this one mutation's primary
effect is to increase radicals [which it is, via messing up Cu
metabolism] then radicals cause aging. But this argument doesn't need
the HGP anyways, so the result is no big deal to me. Still, its nice
that the WSJ has someone who cares about aging because it suggests
that finding startup money for an R&D aging company might not be such
a long shot after all.) Can't recall for sure though.
--Jason
______________________________________________________________________________
Jason Taylor, Greenbelt, MD USA|"Doctor, don't cut so deep! That's the third
http://www.wam.umd.edu/~theoblit| operating table you've ruined this week!"
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To: ageing at net.bio.net
From: theoblit at wam.umd.edu (Jason Taylor)
Subject: Re: New aging insights in Science?
Followup-To: sci.life-extension,bionet.molbio.ageing
Date: 24 Apr 1996 19:13:07 GMT
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